Oleh RENTA SAUT MARULI SIANTURI, S.

Kp
Kel 7: ania, puji, tere, nana, wita,mia
 Defenition
• Acute renal failure is a rapid decrease in renal function
over days to weeks, causing an accumulation of
nitrogenous products in the blood (azotemia).
(www.kidney fun.org /American Kidney )
• Acute renal failure (also called acute kidney injury)
means that your kidneys have suddenly stopped
working
• Acute
– sudden onset
– rapid reduction in urine output
– Usually reversible
– Tubular cell death and regeneration
ANATOMY OF KIDNEY
PHYSIOLOGY
Aliran darah di ginjal
Etiology???
 Masalah Penyebab Yg Mungkin

 Kekurangan darah akibat perdarahan, dehidrasi atau cedera fisik yg

Berkurangnya aliran menyebabkan tersumbatnya pembuluh darah
 Daya pompa jantung menurun (kegagalan jantung)
darah ke ginjal
 Tekanan darah yg sangat rendah (syok)
 Kegagalan hati (sindroma hepatorenalis)

Penyumbatan aliran  Pembesaran prostat

kemih  Tumor yg menekan saluran kemih

 Reaksi alergi (misalnya alergi terhadap zat radioopak yg digunakan

pada pemeriksaan rontgen)
 Zat-zat racun
Trauma pada ginjal
 Keadaan yg mempengaruhi unit penyaringan ginjal (nefron)
 Penyumbatan arteri atau vena di ginjal
 Kristal, protein atau bahan lainnya dalam ginjal
 Causes of ARF
• Pre-renal =
– vomiting, diarrhea, poor fluid intake, fever, use of
diuretics, and heart failure
– cardiac failure, liver dysfunction, or septic shock
• Intrinsic
– Interstitial nephritis, acute glomerulonephritis, tubular
necrosis, ischemia, toxins
• Post-renal =
– prostatic hypertrophy, cancer of the prostate or
cervix, or retroperitoneal disorders
– neurogenic bladder
– bilateral renal calculi, papillary necrosis, coagulated
blood, bladder carcinoma, and fungus
 Fase klinis GGA
1. Initiating phase
adanya pencetus s/d timbul gejala oliguria
2. Oliguria (Vol. Urin <400 cc/hari)1-2 minggu
peningkatan BUN, creatinin, as. Organik,as.
Organik,as. Urat, magnesium, potasium.
Problem
 retensi cairan
 Hiperkalemi, hipermagnesia
 Asidosis metabolik
 Resti infeksi
 Perdarahan saluran cerna
 Perubahan nutrisi
 Resti drug toxicity
3. Diuresis : “self limiting diuresis” (1-2 mgg);
output urin 1-3 L/hari
Problem
 defisit volume cairan tubuh
 hipokalemia
 alkalosis metabolik
4. Pemulihan: GFR normal (6-12 bln)/ kronik
Problem
Pengetahuan episode ARF
 follow-up care
Pencegahan episode berulang
What are the symptoms?
Symptoms of acute renal failure may include:
Little or no urine when you urinate.
Swelling, especially in your legs and feet.
Not feeling like eating.
Nausea and vomiting.
Feeling confused, anxious and restless, or sleepy.
Pain in the back just below the rib cage. This is called flank pain.
Some people may not have any symptoms.
weakness, seizures, confusion, and coma; asterixis and
hyperreflexia may be present on examination. Chest pain (typically
worse with inspiration or when recumbent), a pericardial friction
rub, and findings of pericardial tamponade may occur if uremic
pericarditis is present. Fluid accumulation in the lungs may cause
dyspnea and crackles on auscultation.
 Assesment
• HISTORY:
• Take note of the following findings during the physical
examination:
– Hypotension
– Volume contraction
– Congestive heart failure
– Nephrotoxic drug ingestion
– History of trauma or unaccustomed exertion
– Blood loss or transfusions
– Evidence of connective tissue disorders or autoimmune
diseases
– Exposure to toxic substances, such as ethyl alcohol or ethylene
glycol
– Exposure to mercury vapors, lead, cadmium, or other heavy
metals, which can be encountered in welders and miners
• People with the following comorbid
conditions are at a higher risk for developing
ARF:
– Hypertension
– Congestive cardiac failure
– Diabetes
– Multiple myeloma
– Chronic infection
– Myeloproliferative disorder
Orang dengan riwayat adanya penyakit pada ginjal,
spt glomerulonefritis, hiperplasi prostat, etc
 Physical Assesment
• Skin
– Petechiae, purpura, ecchymosis, and livedo reticularis
provide clues to inflammatory and vascular causes of AK
– Infectious diseases, thrombotic thrombocytopenic purpura
(TTP), disseminated intravascular coagulation (DIC), and
embolic phenomena can produce typical cutaneous
changes.
• Eyes
– Evidence of uveitis may indicate interstitial nephritis and
necrotizing vasculitis.
– Ocular palsy may indicate ethylene glycol poisoning or
necrotizing vasculitis.
– Findings suggestive of severe hypertension, atheroembolic
disease, and endocarditis may be observed on careful
examination of the eyes.
• Cardiovascular system
– The most important part of the physical examination is the
assessment of cardiovascular and volume status.
– The physical examination must include pulse rate and blood
pressure recordings measured in both the supine position and the
standing position; close inspection of the jugular venous pulse;
careful examination of the heart, lungs, skin turgor, and mucous
membranes; and assessment for the presence of peripheral
edema.
– In hospitalized patients, accurate daily records of fluid intake and
urine output and daily measurements of patient weight are
important.
– Blood pressure recordings can be important diagnostic tools.
– Hypovolemia leads to hypotension; however, hypotension may
not necessarily indicate hypovolemia.
– Severe congestive cardiac failure (CHF) may also cause
hypotension. Although patients with CHF may have low blood
pressure, volume expansion is present and effective renal
perfusion is poor, which can result in AKI.
– Severe hypertension with renal failure suggests renovascular
disease, glomerulonephritis, vasculitis, or atheroembolic disease.
 Pemeriksaan laboratorium
• 1. Darah : ureum, kreatinin, elektrolit, serta osmolaritas.
2. Urin : ureum, kreatinin, elektrolit, osmolaritas, dan berat jenis.
3. Kenaikan sisa metabolisme proteinureum kreatinin dan asam urat.
4. Gangguan keseimbangan asam basa : asidosis metabolik.
5. Gangguan keseimbangan elektrolit : hiperkalemia, hipernatremia atau
hiponatremia, hipokalsemia dan hiperfosfatemia.
6. Volume urine biasanya kurang dari 400 ml/24 jam yang terjadi dalam 24
jam setelah ginjal rusak.
7. Warna urine : kotor, sedimen kecoklatan menunjukan adanya darah, Hb,
Mioglobin, porfirin.
8. Berat jenis urine : kurang dari 1,020 menunjukan penyakit ginjal, contoh :
glomerulonefritis, piolonefritis dengan kehilangankemampuan untuk
memekatkan; menetap pada 1,010menunjukan kerusakan ginjal berat.
9. PH. Urine : lebih dari 7 ditemukan pada ISK., nekrosis tubular ginjal, dan
gagal ginjal kronik.
10. Osmolaritas urine : kurang dari 350 mOsm/kg menunjukan kerusakan
ginjal, dan ratio urine/serum sering 1:1.
11. Klierens kreatinin urine (CCT): mungkin secara bermakna
menurun sebelum BUN dan kreatinin serum menunjukan
peningkatan bermakna.
12. Natrium Urine : Biasanya menurun tetapi dapat lebih dari 40
mEq/L bila ginjal tidak mampu mengabsorbsi natrium.
13. Bikarbonat urine : Meningkat bila ada asidosis metabolik.
14. SDM urine : mungkin ada karena infeksi, batu, trauma, tumor,
atau peningkatan GF.
15. Protein : protenuria derajat tinggi (3-4+) sangat menunjukan
kerusakan glomerulus bila SDM dan warna tambahan juga ada.
Proteinuria derajat rendah (1-2+) dan SDM menunjukan infeksi
atau nefritis interstisial. Pada NTA biasanya ada proteinuria
minimal.
16. Warna tambahan : Biasanya tanpa penyakit ginjal ataui infeksi.
Warna tambahan selular dengan pigmen kecoklatan dan sejumlah
sel epitel tubular ginjal terdiagnostik pada NTA. Tambahan warna
merah diduga nefritis glomular.
 Pemeriksaan darah
1. Hb. : menurun pada adanya anemia.
2. Sel Darah Merah : Sering menurun mengikuti peningkatan
kerapuhan/penurunan hidup.
3. PH : Asidosis metabolik (kurang dari 7,2) dapat terjadi karena penurunan
kemampuan ginjal untuk mengeksresikan hidrogen dan hasil akhir metabolisme.
4. BUN/Kreatinin : biasanya meningkat pada proporsi ratio 10:1
5. Osmolaritas serum : lebih beras dari 285 mOsm/kg; sering sama dengan urine.
6. Kalium : meningkat sehubungan dengan retensi seiring dengan perpindahan
selular ( asidosis) atau pengeluaran jaringan (hemolisis sel darah merah).
7. Natrium : Biasanya meningkat tetapi dengan bervariasi.
8. Ph; kalium, dan bikarbonat menurun.
9. Klorida, fosfat dan magnesium meningkat.
10. Protein : penurunan pada kadar serum dapat menunjukan kehilangan protein
melalui urine, perpindahan cairan, penurunan pemasukan, dan penurunan
sintesis,karena kekurangan asam amino esensial
11. CT.Scan
12. MRI
13. EKG mungkin abnormal menunjukan ketidakseimbangan elektrolit dan
asam/basa.
 Komplikasi
Possible Complications
• Chronic (long-term) kidney failure
• Damage to the heart or nervous system
• End-stage kidney disease
• High blood pressure
• Loss of blood in the intestines
 Acute Renal Failure Management
• Make/think about the diagnosis
• Treat life threatening conditions
• Hipoperfusi renal:
- Normovolemia : resusitasi cairan CVP 12
- Normotensi: norepinefrin
- furosemid
• Identify the cause if possible
– Hypovolemia
– Toxic agents (drugs, myoglobin)
– Obstruction
• Treat reversible elements
– Hydrate
– Remove drug
– Relieve obstruction
 Nursing Diagnosis
• 1. Perubahan kelebihan volume cairan b/d gagal ginjal dengan
kelebihan air.
2. Resiko tinggi terhadap menurunnya curah jantung
berhubungan dengan ketidakseimbangan cairandan elektrolit,
gangguan frekuensi, irama, konduksi jantung,
akumulasi/penumpukan urea toksin, kalsifikasi jaringan lunak.
3. Gangguan pemenuhan nutrisi kurang dari kebutuhan tubuh
berhubungan dengan katabolisme protein
4. Kelelahan berhubungan dengan penurunan produksi energi
metabolik/pembatasan diet, anemia.
5. Resiko tinggi terhadap infeksi b/d depresi pertahanan
imunologi.
6. Resiko tinggi terhadap kekurangan volume cairan b/d
kehilangan cairan berlebihan.
7. Kurang pengetahuan tentang kondisi,prognosis dan
kebutuhan pengobatan b/d kurang mengingat.